To establish a set of eminently practical recommendations on the management of PsA for both rheumatologists and dermatologists.

• 1.

  To review the tools for screening, assessment, and classification of PsA recommended in the main guidelines and to indicate those most appropriate for each specialty (rheumatology and dermatology) and clinical situation.

• 2.

  To develop diagnostic and treatment algorithms for the coordinated management of PsA by dermatologists and rheumatologists.

• 3.

  To establish guidelines and recommendations for the coordinated management of PsA.

Fig. 1 is a detailed algorithm showing the procedure that should be used by dermatologists to screen for PsA.

Figure 1.

Screening for psoriatic arthritis in the dermatology office. PsA indicates psoriatic arthritis; BSA, % affected body surface area; PASI, Psoriasis Area and Severity Index.

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In the clinical examination of a patient with psoriasis, the dermatologist should include screening for PsA at regular intervals. This is particularly important in patients with risk factors for PsA, such as onychopathy, obesity, extensive skin disease (>3areas affected by psoriasis), or involvement of sites such as the scalp and intergluteal cleft.

As mentioned in the publications of the AEDV Working Group on Comorbidity in Psoriasis,23,24 the CASPAR criteria are difficult to apply in clinical practice outside the rheumatology office because they require diagnosis of inflammatory arthritis and radiographic evidence of juxtaarticular new bone formation (excluding osteophyte formation). To address this problem, the working group proposed criteria for referral to a rheumatologist based on a simplified version of the CASPAR criteria (Table 3). These modified criteria are indicative of suspected PsA rather than a confirmed diagnosis.

To apply this simplified adaptation of the CASPAR criteria, dermatologists must collect information on the presence or absence of the following signs and symptoms: inflammatory musculoskeletal pain (Table 4), current swelling of the peripheral joints (especially the knees, ankles, and the small joints of the hand), inflammatory or nocturnal pain in the axial skeleton (Table 5) or zones of tendon insertion, especially on the heels (Achilles tendon) and soles of the feet (plantar fascia).34 They must perform a visual inspection and exploration of suspect joints and entheses for redness, heat, limitation of mobility, swelling, and pain. The limbs should be examined to identify psoriatic onychopathy (nail dystrophy, onycholysis, pitting, or hyperkeratosis) or dactylitis (“sausage digits”, that is, swelling of an entire digit).23

When a patient diagnosed with PsA is referred to the dermatologist, the skin specialist will perform a thorough examination to look for psoriasis, paying particular attention to the sites most often associated with PsA (nails, scalp, intergluteal region, etc.). The dermatologist should then provide the rheumatologist with a report on the patient's psoriasis, including a proposal for coordinated management of the two conditions.

Certain skin lesions—especially palmoplantar pustulosis associated with musculoskeletal pain (mainly when this is located in the anterior thorax, but also when it affects the dorsal spine or unilateral sacroiliac joint, or takes the form of a monoarthritis affecting a large joint)—require a differential diagnosis with SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis). The dermatologist will study the skin lesions and refer the patient to a rheumatologist, who will study and classify the type of musculoskeletal disease.

The algorithm in Fig. 2 shows the procedure that should be used by rheumatologists to screen for PsA.

Figure 2.

Screening for psoriatic arthritis in the rheumatology office. PsA indicates psoriatic arthritis; PASI, Psoriasis Area and Severity Index; BSA, % of body surface area affected; MRI, magnetic resonance imaging; Rx, radiography.

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A suspected diagnosis of PsA may be established in the rheumatology consultation either in a patient with psoriasis referred by a dermatologist or in a patient (with or without psoriasis) who consults a rheumatologist for articular pain (joint or spine), dactylitis, and/or enthesitis. The CASPAR criteria (particularly when peripheral PsA is suspected),29 together with sacroiliac radiography and assessment of vertebral mobility (to detect axial PsA),27 can be useful in the initial diagnosis. Table 6 lists the GRAPPA criteria for the diagnosis of axial PsA.27 If enthesitis is suspected, Doppler ultrasound and magnetic resonance imaging are useful to complement clinical examination of tendon, ligament, and capsular insertions for pain, inflammation, or tenderness on palpation or pressure.29 Dactylitis, a condition found in between 16% and 48% of patients with psoriatic joint disease, is an indicator of the severity of PsA.35 In some cases, isolated but recurrent episodes of dactylitis may be the only clinical manifestation of PsA.

SAPHO syndrome is one of the disorders the rheumatologist must include in the differential diagnosis. It is an uncommon seronegative rheumatic condition associated with palmoplantar skin lesions of the pustulosis type that predominantly affects the sternocostal and sternoclavicular joints of the anterior chest wall, but can also give rise to sacroiliitis, dorsal vertebral involvement, and synovitis of the large joints. The features that distinguish SAPHO syndrome from PsA include the presence of hyperostosis, predominantly thoracic involvement, unilateral sacroiliac involvement, and nonerosive peripheral oligoarthritis.

If the diagnosis of PsA is confirmed, the rheumatologist should carry out the initial assessment and identify the clinical form. This initial assessment should include a medical history, physical examination, laboratory tests, radiography. Standardized and validated evaluation tools should be used to classify the condition: the DAS28 (Disease Activity Score based on 28joint counts) to establish peripheral PsA involvement and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) in the case of axial disease. The tools used should allow the clinician to measure inflammatory activity, function, and structural damage, as well as the toxicity of treatment and response to therapy. Also of interest is the measurement of aspects—quality-of-life for instance—of vital interest to the patient. The results of this initial assessment will be used to establish criteria for remission and activity. Table 7 summarizes the parameters that should be taken into consideration in the assessment of peripheral PsA. It includes the parameters that should be assessed initially and those that should be taken into account when evaluating response to non-steroidal anti-inflammatory (NSAID), DMARD, or biologic therapy. Table 8 lists the parameters that should be assessed in axial PsA. Both tables include assessment of skin and nail involvement, which, if not provided, should be requested from the dermatologist together with a treatment plan for the skin disease.

The clinical form of PsA is classified on the basis of the results of this initial evaluation. For practical purposes, PsA can be classified according to the predominant component of the joint disease as predominantly peripheral PsA (with or without an axial component) or predominantly axial (with or without a peripheral component). For the purposes of prognosis and treatment, both forms are also stratified according to the level of clinical activity (clinical signs and symptoms and acute-phase reactants), structural damage, functional impairment, and impact on quality-of-life. For the practical purposes outlined in this document, Tables 9 and 10 propose clinical classifications of peripheral and axial psoriatic arthritis based on the guidelines reviewed.27–29

Since the severity of PsA frequently does not correlate with that of psoriasis, the assessment must include a dermatology report, which should include information on the patient's Psoriasis Area and Severity Index (PASI) score and the percentage of body surface area affected (% BSA), as well as the recommended treatment plan for the skin disease. The overall treatment plan should be developed jointly by the two specialists taking into account both joint and skin disease.

The goal of treatment in PsA is to achieve remission of the disease or, at least, minimum disease activity (Table 11). This implies achieving significant improvement in signs and symptoms, preserving functional capacity, maintaining a good quality-of-life, and controlling structural damage.29,36Tables 12–14 list the objectives for each treatment in peripheral and axial PsA.29

NSAIDs, alone or in combination with local injections of corticosteroids, are useful in mild peripheral PsA with skin involvement that responds well to topical therapy (corticosteroids, vitamin D analogs) and UV-B or psoralen-UV-A phototherapy.

If the skin disease has not responded to earlier treatment or requires systemic therapy (Table 15), treatment with DMARDs (alone or in combinations) is recommended. In patients with moderate to severe peripheral PsA, DMARD treatment (monotherapy or in combinations) and even low dose corticosteroids are also recommended. If the patient also has skin disease, caution should be exercised with corticosteroid treatment, which may exacerbate psoriasis.27 In PsA, biologic therapy is indicated when treatment with DMARDs has failed or is contraindicated or the patient is intolerant to such treatment. Fig. 3 presents a treatment algorithm for peripheral PsA based on the SER consensus statement on the use of biologic agents in PsA.29 This algorithm includes criteria for treatment failure and recommendations for evaluating treatment.

Figure 3.

Treatment algorithm for peripheral psoriatic arthritis. NSAID indicates nonsteroidal anti-inflammatory drugs; DMARD, disease-modifying antirheumatic drug; CS corticosteroids; BT, biologic therapy.

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DMARDs with proven efficacy in peripheral PsA include sulfasalazine, methotrexate, leflunomide, and ciclosporinA, although the most highly recommended of these in PsA are methotrexate and leflunomide because of their risk-benefit profile.29 However, since methotrexate is the first-line choice among DMARDs in psoriasis, it is the recommended treatment in patients who have both psoriasis and PsA.37 The treatment regimens for DMARDs in PsA are summarized in Table 16.

In predominantly peripheral PsA, treatment with biologic therapy should be considered when an adequate response has not been obtained following treatment with DMARDs (monotherapy or a combination regimen) for at least 3months, during at least 2 of which the patient must receive the full dose (except when the dose is limited by intolerance or toxicity).29

Treatment with NSAIDs and physiotherapy are the first-line treatment in mild to moderate axial PsA when the skin disease does not require treatment with DMARDs or biologic therapy. However, since DMARDs have not been shown to be effective in axial PsA, biologic therapy is recommended when NSAID treatment fails to produce an adequate response or when the skin condition is refractory to topical therapy or requires systemic therapy. In predominantly axial PsA, biologic therapy is considered when treatment has failed with at least 2 NSAIDS having proven anti-inflammatory effect. In each case, the NSAID must have been administered for at least 4weeks at the maximum recommended or tolerated dose, except when there are contraindications to NSAIDs or evidence of toxicity.29 The treatment algorithm for axial PsA, also based on the SER consensus statement, is presented in Fig. 4.29

Figure 4.

Treatment algorithm for axial psoriatic arthritis. PsA indicates psoriatic arthritis; NSAID, nonsteroidal anti-inflammatory drug; COX-1, cyclooxygenase-1 selective inhibitor; COX-2, cyclooxygenase-2 selective inhibitor.

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Four biologic agents are currently approved by the regulatory agencies for the treatment of the signs and symptoms of active PsA refractory to conventional therapies (Table 17): adalimumab, etanercept, golimumab, and infliximab (Fig. 5).

Figure 5.

Protocol for rapid escalation of methotrexate. MTS indicates methotrexate; DMARD, disease-modifying antirheumatic drug. *If oral treatment is ineffective or not tolerated by the patient, parenteral administration may be considered.

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There is currently insufficient evidence from direct comparisons to support the use of one biologic agent rather than another in the treatment of PsA.38 Consequently the choice of treatment depends on the physician's criteria, the particular circumstances of each patient, and the structure, antigenicity, and mechanisms of action of the different biologic therapies.39 In the databases of international registers and in observational studies, it appears that etanercept may be associated with longer drug survival than other anti-TNF agents in patients with PsA.40–42

If within 3 to 4 months of starting biological therapy no response has been obtained (in polyarticular PsA, a DAS28 higher than 3.2 or between 2.6 and 3.2 without a decline of 1.2points over the previous assessment) or if the initial response has been lost, there is no evidence to support a change in the dose of the current biologic agent. Thus, an alternative treatment strategy should be considered, that is, a switch to another biologic agent. If the response is acceptable (in polyarticular PsA, DAS28 between 2.6 and 3.2 and/or a decrease of 1.2points compared to the previous value), treatment should be continued with the possible addition of a DMARD. If the treatment goal has been achieved, treatment should be continued and response assessed in 3 to 4months.29

There is currently insufficient evidence in patients with PsA receiving biologic therapy whose condition is in remission to support a recommendation for reducing the dose or prolonging the interval between doses, although a reduction in treatment intensity can be considered on a case-by-case basis.29 Some authors have published their experience with dose reduction in this setting.43 This topic is currently considered to be a priority research target.36

As there is very little information in the literature concerning the monitoring and follow-up of patients with PsA,44–46 recommendations are based on expert opinion.

As a general rule, the rheumatologist is in charge of the management of PsA, but the dermatologist who detects signs or symptoms indicative of a worsening of PsA should refer the patient to the rheumatologist. The dermatologist will also agree with the rheumatologist any change in the patient's treatment that might directly affect the course of PsA (in particular changes in DMARD or biologic therapy). Likewise, the rheumatologist will agree with the dermatologist on any change in therapy that might directly affect the course of psoriasis (in particular changes in DMARD or biologic therapy).

The assessment undertaken by the rheumatologist on follow-up of patients with PsA will be shorter and more specific than the initial evaluation; the findings of the physical examination, complete blood count, routine biochemistry, CRP, and ESR together with an assessment of prognosis should all be recorded in the patient's clinical records. The follow-up visit provides an opportunity to assess the activity of PsA and to evaluate adherence and response to treatment and identify any adverse effects.

Tables 7 and 8 list the parameters that should be assessed and the recommended instruments for use in the follow-up of PsA. In order to assess disease activity, objective data will be collected and recorded, including tender and swollen joint counts, the presence of dactylitis or enthesitis, and the physician's global disease assessment. At the same time subjective data will be collected, including the patient's assessment of disease activity and pain during the preceding week using a visual numeric scale (VNS). The results of laboratory tests indicative of inflammation, such as CRP and ESR, will also be recorded together with an assessment of the impact of the disease on the patient's social and working life (asthenia, functional capacity, quality-of-life). It may also be useful to record information on the use of symptomatic treatments. Use of the DAS28 to assess treatment response is recommended in polyarticular forms in spite the limitations of the instrument. Although the DAS28 was developed specifically to assess rheumatoid arthritis, the rheumatologist's familiarity with its use and the fact that the calculator can measure response to treatment make it an attractive tool for monitoring polyarticular forms of PsA in routine practice. The BASDAI is the recommended method for assessing treatment response in axial PsA. Monitoring aimed at identifying adverse effects to therapy should include complete blood count and routine biochemistry in addition to the specific tests required for each drug.

The results of skin and nail assessment should also be recorded, especially in moderate to severe psoriasis. The patient should be referred to a dermatologist for a report on PASI and BSA scores and to obtain a proposed treatment plan if this is considered clinically necessary.

Radiographs of symptomatic joints must be obtained during patient follow-up. Anteroposterior radiographs of the hands and feet should be obtained if the PsA is polyarticular. These should be obtained annually for the first 3 to 4years after onset, after which the frequency will depend on disease activity.

If the disease is well controlled and not acute and the patient does not require special monitoring related to the drug regimen or other circumstances, follow-up visits should be scheduled every 6 to 12months. When it is necessary to establish the effectiveness of a therapeutic intervention or monitor compliance, or when the clinical situation demands more frequent consultations, follow up visits should be scheduled every 4 to 6weeks for up to 4months after start of treatment or stabilization of symptoms.

Biologic therapy occasionally triggers a paradoxical reaction that can provoke an exacerbation of existing lesions or de novo psoriasis in patients with no prior skin involvement. These flares of psoriasis associated with biologic therapy can appear within days of the start of anti-TNF therapy or after years of treatment. The most common presentation is palmoplantar psoriasis, either pustular or hyperkeratotic. The choice of treatment in such cases will depend on the extent of the lesions and their response to topical treatment. Tolerable lesions with a BSA of less than 5% to 10% should be treated topically with corticosteroids, keratolytic agents, or vitamin D analogs. If the condition does not improve, switching to another biologic agent or discontinuation of biologic therapy should be considered. If the lesions are tolerable but the BSA is greater than 5% to 10% or the patient has palmoplantar involvement, a switch to another biologic agent and the addition of topical therapy with occlusive corticosteroids in combination with phototherapy, acitretin, and/or a DMARD (MTX or ciclosporin A) may be considered; if the problem does not improve, a switch to another biologic agent or discontinuation of biologic therapy should be considered. When the lesions are more severe or the patient finds them intolerable or wishes to discontinue the treatment regimen, biologic therapy should be discontinued and topical treatment initiated. The rheumatologist should refer to the dermatologist any patients receiving treatment with biologic therapy who develop skin disease or experience worsening of existing lesions.47,48 If de novo psoriasis develops or existing psoriasis is exacerbated, the dermatologist will propose an appropriate treatment plan to the rheumatologist, taking into account the severity and extent of the skin involvement.

Communication between the primary care physician, dermatology and rheumatology should be prompt and efficient.

The authors declare that no experiments were performed on humans or animals for this investigation.

The authors declare that no private patient data are disclosed in this article.

The authors declare that no private patient data are disclosed in this article.